CLINICAL

DEMONSTRATION
TOPIC: ELECTROCARDIOGRAM

(ECG)

Submitted to, Submitted by,

Prof. Shashikumar Jawadagi Miss. Soniya Joseph

HOD 1st MSc Nursing

Dept. Medical Surgical Nursing Yenepoya Nursing College

Submitted on: 15/07/19

INTRODUCTION

The electrical conduction system of the heart is composed of sinoatrial (SA) node, internodal
atrial conduction tracts, interatrial conduction tract, atrioventicular (AV) node, bundle of HIS,
right and left bundle branches, and Purkinje network. The AV node and the bundle of HIS
form the AV junction. The bundle of HIS, the right and left bundle branches, and the
Purkinje network are also known as the HIS-Purkinje system of the ventricles. As its sole
function, the electrical conduction system of the heart transmits minute electrical impulses
from the SA node (where they are normally generated) to the atria and ventricles, causing
them to contract.

The SA node lies in the wall of the right atrium near the inlet of the superior vena cava and
consists of pacemaker cells that generate electrical impulses automatically and regularly. The
AV node lies partly in the right side of the interatrial septum in front of the opening of the
coronary sinus tricuspid valve.

ELECTRICAL BASIS OF THE EKG

The electrocardiogram, ECG, is a graphic record of the direction and magnitude of the
electrical activity that is generated by the depolarization and repolarization of the atria and
ventricles. This electrical activity is readily detected by the electrodes attached to the skin.
In the next section we will go into more detail about the EKG tracing and the normal EKG.
This will lay a foundation for interpretation of arrhythmias to come later.

We use EKG – ECG interchangeably. They mean the same thing. EKG was a term
originated from old English, and is still used today. Some facilities prefer one term over the
other. Use the term that is preferred at your facility.

THE ELECTROCARDIOGRAM AND THE NORMAL EKG

The ECG Paper and the Normal ECG Tracing

In order to begin to understand the interpretation of EKC’s one must have an understanding
of the EKG paper. Shown in the illustration below are a sample of EKG paper and an
enlargement of the markings. The time intervals are shown as well as the measurements of
each block on the paper. You will be able to make fairly accurate measurements of the
patient’s heart rate and other measurements by counting blocks up and down on the paper.

The EKG paper records time sequences (horizontal deflections) and amplitude (vertical
deflections) of the electrical activity of the heart. The horizontal lines measure time intervals
and heart rate. Each of the small squares equal 0.4 second of time. Five small squares equal
0.20 seconds. Fifteen of the 0.20 squares represent 3 seconds. These 3 – second time
intervals are marked on the paper by darker lines as shown below.
 Fig:1 : Normal ECG

COMPONENTS OF NORMAL SINUS RHYTHM

P Wave:

The P wave represents depolarization of the right and left atria.

Onset of the P Wave is identified as: the first abrupt or gradual deviation from the baseline.
The point where the wave returns to the baseline marks the end of the P Wave. A QRS
complex normally follows each P Wave. A normal sinus P Wave indicates that the electrical
impulse responsible for the P Wave originated in the SA node and that normal depolarization
of the right and left atria has occurred.

1. SA node is the pacemaker site.

2. The first part of the normal sinus P Wave represents depolarization of the right atrium; the
second part represents depolarization of the left atrium.

3. During the P Wave, the electrical impulses progress from the SA node through the
intermodal atrial conduction tracts and most of the AV node.

4. The DIRECTION of the P Wave in lead II is positive (upright).

5. The DURATION is 0.10 seconds or less.

6. The AMPLITUDE is 0.5 to 2.5 mm high, in lead II (rarely over 2mm high)

7. The SHAPE is normally smooth and rounded.

8. The P-R INTERVAL is normally 0.12 to 0.20 seconds; abnormal is greater than 0.20
seconds.

QRS COMPLEX

A QRS Complex represents depolarization of the right and left ventricles.

The pacemaker site of a normal QRS complex is the SA node or an ectopic pacemaker in the
atria of AV junction. (The origin of the QRS is originally from the SA node, and then
spreads down through the atria to the AV node, etc.) The onset of the QRS Complex is
identified as the point where the first wave of the complex just begin to deviate, abruptly or
gradually, from the baseline.

This end of the QRS Complex is the pone there the last wave of the complex begin to flatten
out, sharply or gradually, at, above, or below the baseline. This point the junction between the
QRS complex and the S-T segment is called the “JUNCTION” or “J POINT.” A normal
QRS Complex indicates that the electrical impulse has progressed normally from the bundle
of HIS to the Purkinje network through the right and left bundle branches, and that normal
depolarization of the right and left ventricles has occurred. Of course, there can be several
“normal” variations of the QRS Complex. These will be discussed later in the course.

1. The Q Wave is the first negative deflection in the QRS Complex not preceded by an R
Wave.
2. The R Wave is the first positive defection in the QRS Complex
3. The S Wave is the first negative deflection that extends below the baseline in the QRS
Complex that follows the R Wave
4. The DURATION of the QRS Complex is 0.06 to 0.10 seconds in adults and 0.08 or
less in children.

T Wave

A T Wave represents ventricular repolarization.

Repolarization of the ventricles begins at the epicardial surface of the ventricles and
progresses inwardly through the ventricular walls to the endocardial surface. The T Wave
occurs during the last part of the ventricular systole. The onset of the T Wave is the first or
abrupt or gradual deviation from the S-T segment; or from the point where the slope of the S-
T segment appears to become abruptly of gradually steeper. If the S-T segment is absent, the
T Wave begins at the end of the QRS Complete (or the J Point). The point where the T Wave
returns to the baseline marks the end of the T Wave. Often the onset and end of the T Wave
are difficult to determine with certainty.

1. The DURATION of the T Wave is 0.10 to 0.25 seconds or greater.

2. The AMPLITUDE of the T Wave is less than 5 mm.

3. The SHAPE of the T Wave is sharply or bluntly rounded and slightly asymmetrical.

4. A T Wave always follows a QRS Complex.

THE U WAVE

The U Wave probably represents the final state of repolarization of the ventricles.

The U Wave probably represents repolarization of a small segment of the ventricles, such as
the papillary muscles or ventricular septum, after most of the right and left ventricles have
been repolarized. Although uncommon, and not easily identified, the U Wave can best be
seen when

the heart rate is slow. A U Wave indicates that the repolarization of the ventricles has
occurred. An abnormally tall U wave may be present in hypokalemia, cardiomyopathy, left
ventricle hypertrophy, diabetes, and may follow administration of digitalis and quinidine.

1. The ONSET of the U wave is identified as the first abrupt or gradual deviation from the
baseline or the downward slope of the T Wave.

2. The END of the U Wave is the point where it returns to the baseline or downward slope of
the P Wave.

3. The DIRECTION of the U Wave is positive (upright), the same as that of the preceding
normal T Wave in lead II. An abnormal U Wave may be flat or inverted.

4. The DURATION of the U Wave is normally not determined and the duration is normally
not significant, except in rare cases.

5. The AMPLITUDE of a normal U Wave is usually less than 2mm and always smaller than
that of the preceding T Wave in lead II.

6. The U Wave always FOLLOWS the peak of the T Wave and occurs before the next P
Wave.
THE EKG LEADS

The 12-lead EKG will be discussed in greater detail later in this course. However, at this
time we will present an introduction to the EKG leads simply to help explain the basics of
EKG interpretation that will follow. Later, the specifics of leads and lead placement will be
discussed.

An EKG lead consists of two surface electrodes of opposite polarity (positive and negative)
or one positive surface electrode and one reference point. A lead composed of two electrodes
of opposite polarity is called a Bipolar Lead. A lead composed of a single positive electrode
and a reference point is called a Unipolar Lead.

All leads of the ECG record the same electrical impulses of the heart muscle. However, each
lead placed in a different area of the body, records the electrical activity from a slightly
different “angle.” This means that by using the ECG tracing from different positions of the
chest, various ECG waves will be accentuated. Diagnosis of arrhythmias may be made easier
by examination of different leads. The 12-lead ECG tracing is standard. Six leads are
recorded by placing wires on each limb. The other six leads are recorded by placing wires on
the chest in six specific positions.

Limb Leads: I, II, III, IV, V, VI Lead IV also called AVR Lead V also called AVL Lead
VI also called AVF .

CHEST LEADS:

For diagnosis of most arrhythmias, lead II is most commonly used. Lead II (and the chest
leads) most consistently show the most clear P Wave which can be diagnostic of many
common arrhythmias.
 Fig:2: Conduction in ECG

NORMAL SINUS RHYTHM

Normal Sinus Rhythm, NSR, is the term used to describe the normal heartbeat. Looking at
the EKG tracing, all beats appear similar and are evenly spaced. The NSR implies that all of
the beats have a normal pacemaker (starts at the SA node). All of the beats also follow the
normal conduction pathways in NSR. Lastly, all components of the waves are similar, the P
Wave, QRS Complex, and T Wavers are similar to each other.

Arrhythmias

The normal EKG consists of repetitive series of P, Q, R, S, and T Waves, which conform to
established standards for size and shape and occur 60 – 100 times each minute. If these
conditions prevail, the heart is in normal sinus rhythm. When either the rate of the contour of
any of the individual waves is abnormal, the disorder is called an arrhythmia.

CLASSIFICATIONS OF ARRHYTHMIAS:
There are several ways in which arrhythmias may be classified. Perhaps the most logical
method involves classification, first, by the site of the arrhythmia and secondly by the type of
mechanism responsible for the disorder.

Sites Mechanisms SA Node (sinus rhythms) Tachycardia (rate over 100 bpm) Atrial (atrial
rhythms) Bradycardia (rate under 60 bpm) AV node (nodal rhythms) Premature beats
Ventricles (ventricular rhythms) Flutter Fibrillation Defects in conduction.

Arrhythmias can also be classified in a general way according to their seriousness or

prognosis. This is a meaningful method for nurses caring for patients with acute Myocardial
Infarction and the one we have found useful.

Using this division, arrhythmias may be considered as:

1. Minor – these arrhythmia are not of the immediate concern and generally do not affect
circulation. They are important because they frequently reflect irritability of the heart.

2. Major – these disturbances reduce the efficiency of the heart of warn of impending danger
and require prompt treatment.

3. Death Producing – Immediate resuscitation is needed to prevent death.

IDENTIFYING ECG FEATURES – SINUS ARRHYTHMIAS

1. Rate (In Sinus Arrhythmias) The heart rate per minute is normal (60-100); however, the
rate increased during inspiration and then slows during expiration.

2. Rhythm (In Sinus Arrhythmias) Irregular rhythm; there is a variation of at least 0.12
seconds between the longest and shortest R-R intervals.

3. P Waves (In Sinus Arrhythmias) P Waves are normal.

4. PR Interval (In Sinus Arrhythmias) Normal; each P Wave is followed by a normal QRS
complex.

5. QRS (In Sinus Arrhythmias) QRS is normal width

SINUS BRADYCARDIA
Sinus Bradycardia is an arrhythmia defined as a rate below 60 BPM with all beats remaining
normal. The SA node is still the pacemaker and the conduction pathway is still normal. This
rhythm can be normal during sleep, for athletes, for persons on certain medications and other
reasons. It can be an abnormal rhythm in certain conditions such as myocardial infarction or
congestive heart failure, or if the rate falls so low as to cause clinical symptoms such as
fainting of dizziness, etc.

SINUS TACHYCARDIA

Sinus tachycardia is another sinus arrhythmia. Causes of this condition are exercise, anxiety,
fear, fever, and others. If the tachycardia is secondary to another factor, such as above,
usually no treatment is needed, as these conditions are usually temporary. However, if
clinical signs are seen, such as dizziness, fainting, or others, treatment may be indicated and
perhaps more than just simple sinus tachycardia is present.

ABNORMAL RHYTHMS

A. ATRIAL ARRHYTHMIAS

1. Atrial Tachycardia and Paroxysmal Atrial Tachycardia (PAT)

PAT is a relatively common arrhythmia in young adults and usually means no permanent
heart damage. Many young adults experience brief episodes of “fluttering” or “pounding” in
the chest that also may cause a short period of weakness. The episode may be so brief that it
goes almost unnoticed.

On the ECG, PAT will be seen as the heart beating at a rate of 160 to 240 Beats per Minute
(BPM). The P Wave will be shaped differently than the normal P wave. When the impulses
from the SA node travel the normal pathway to the AV node, the ECG shows a “normal P
wave.” However, when PAT is present, the pacemaker is not the normal SA node. The P
wave has a different shape due to this fact.

By definition, PAT commonly starts and ends abruptly (in paroxysms). Atrial Tachycardia is
defined as three or more consecutive (abnormal) atrial contractions. Atrial Tachycardia then,
is sustained abnormal atrial contractions. Therefore, PAT is defined as just an occasional
abnormal atrial contraction (fewer than three in a row).
Supraventricular Tachycardia is a term used to indicate a paroxysmal tachycardia originating
in the atria of AV junction without specifying the exact location of the ectopic pacemaker
site.

Many times is difficult to determine the site so the arrhythmia is called supraventricular
tachycardia.

As you see from the previous PAT example, there is an abnormal pacemaker that sends
impulses to the AV node. The ventricular wave (QRS) appears normal but rapid in response
to the rapid atrial stimulation. To summarize, PAT is recognized by a rate of over 140 per
minute (higher than sinus tachycardia), normal QRS complexes and abnormally shaped P
Waves when they are visible and not hidden by the preceding T Wave.

TREATMENT OF PAT

As we mentioned earlier, PAT will often stop spontaneously and requires no treatment. IN
more severe cases, which are either prolonged or case clinical symptoms, treatment is
required. In these severe cases, the ECG machine will remain attached to the patient because
many of the treatments for PAT can in themselves cause cardiac complications. The simplest
form of treatment may be the administration of a sedative or tranquilizer. In ten to fifteen
minutes, the episode may terminate. This procedure stimulates the heart-slowing vagus nerve
and may break the episode of PAT. Gagging the patient with a tongue depressor may
accomplish the same thing.

In cases where none of the above drugs may be used due to the patient’s condition,
cardioversion (administering a synchronized electric shock) may be useful. The shock
delivered stops the heart momentarily and then allows the normal pacemaker of the heart to
take over. For most cases of PAT, however, the drug therapy with Aramine works quite well.

2. ATRIAL FLUTTER

This arrhythmia is similar to PAT in origin. The pacemaker for flutter is also located on one
spot in the atrium, usually in the lower atrium near the AV node. The rate for flutter,
however, is faster than PAT, 250-350 per minute. Another difference with flutter is that not
all of the P waves cause conduction of the ventricles and subsequent contraction. In PAT
each rapid P wave caused ventricular responses, there was no blockage of the electrical
impulses. However, with atrial flutter, P waves come too fast for each of them to cause a
ventricular contraction.

Atrial flutter is usually treated by digitalization. The digitalis slows the pulse rate by blocking
the impulses at the AV node so that fewer impulses get through to the ventricles. Some
persons with this arrhythmia have no clinical symptoms. Other persons become weak and
dizzy, and then can develop symptoms of congestive heart failure. The heart cannot work
effectively if the ventricular rate is too rapid.

If the patient does exhibit any adverse symptoms which suggests possible danger, another
treatment may be used; cardio version. Cardio version is also used if digitalization fails to
convert the patient to a normal sinus rhythm within a safe period of time. This cardio version
uses 20 to 50 watt-seconds.

3. ATRIAL FIBRILLATION

This arrhythmia occurs due to multiple electrical impulses leaving the atrium.
Arteriosclerosis and other diseases can cause scarring of the atrium. This scar tissue becomes
“irritable” and begins to send out many impulses across the atria. The ECG tracing will not
show a distinct P wave since the rate is extremely rapid (350-600). The P waves appear as an
atrial wave or in other words, wavering lines with no distinct P wave visible (see figure
below). The patient’s pulse is irregular. Since the P waves come so rapidly and at irregular
intervals, the ventricular response is irregular and so is the pulse usually.

The patient may or may not have clinical symptoms. Some patients have weakness and
hypotension, other patients have no symptoms. The ventricular response usually determines
if the patient will by symptomatic or not. If the AV node blocks large numbers of the P
waves, the ventricles will then maintain a fairly normal pulse. If the AV node allows many P
waves through, the ventricles will respond and the pulse can become very high. As the
ventricles respond faster to the P wavers, cardiac output will decrease and the patient may
then become symptomatic.

This is A.F. with slow ventricular response. Note the “wavy” appearance of the multiple
rapid P waves.

As mentioned, when the patient’s pulse rate reaches and passes 100 beats per minute, cardiac
output usually begins to drop due to incomplete filling of the ventricles. When the symptoms
begin to appear, the patient must be treated, or it may lead to CHF and other complications.
If the patient is not already on digitalis, treatment for atrial fibrillation (AF) is digitalization.

This therapy takes several hours, so the patient should be in a stable condition. If digitalis
therapy is not practical for some reason, cardio version may be necessary. Cardio version
does have risk involved, especially if the patient is already on digitalis. One hundred watt-
seconds is usually used for this purpose.

Other treatment methods for AF include the use of quinidine and propranolol. There are also
some new drugs which will be available soon to treat this arrhythmia.

4. PREMATURE ATRIAL CONTRACTIONS (PAC’S)

PAC’s are ectopic discharges from the atrium causing contraction of the atrium. However,
there is not always ventricular contraction following these discharges. The focus of the
discharge may be either the right or left atrium. The QRS is almost always normal, but may
be aberrantly conducted. Rare PAC’s occur normally in most people, but frequent ones may
be indicative of organic heart disease.

The treatment of PAC’s depends upon the frequency of occurrence and the clinical symptoms
involved. Usually mild conditions respond to the omittance of stimulants from the diet or to
stopping certain drug therapies for example: caffeine, tobacco, amphetamines, alcohol, etc.
Mild sedation may also be used to stop mild episodes. In more severe cases, and in cases
where there are severe clinical signs/symptoms, drug therapy may be indicated. Drugs
commonly used to stop PAC’s include digitalis, quinidine, propranolol and procainamide.

5. JUNCTIONAL (NODAL) CONTRACTIONS (ALSO KNOWN AS PREMATURE

JUNCTIONAL CONTRACTIONS, PJC’S)

Just as the name implies, the disorder is causes by a premature contraction. The pacemaker
site of the PJC is an ectopic pacemaker in the AV junction. The rhythm is irregular when the
premature contractions are present. P Waves may or may not be associated with PJC’s. If
they are present, they are abnormal, varying in size, shape, and direction from the normal P
Waves. The P Waves are often inverted when present, or they are buries in the QRS complex
so they are not visible.

Occasional PJC’s may occur in a healthy person without a specific cause. However, PJC’s
are most often caused by digitalis toxicity, excessive doses of other cardiac drugs, and by
enhanced automaticity of the AV junction. PJC’s often resemble PVC’s (discussed later).
Therefore, they must be identified properly in order to have the correct treatment given.

6. AV BLOCK

AV Block refers to several different related arrhythmias. The name itself sounds innocent,
but several of the related disorders may be life-threatening. By definition, AV Block refers to
a disorder of the AV node. There is scarring or inflammation at the node and impulses are
slowed or blocked at that point. If the heart block is total or complete, no impulses get
through to the ventricles in order to initiate their contraction. AV Block is described in three
“stages” in order of the amount of blockage present. There is first degree block, second
degree block, and third degree block. Each degree higher represents more severe blockage.

FIRST DEGREE AV BLOCK

First Degree AV Block is the least serious condition of the three. It is characterized by a
prolonged conduction of the impulses through to the ventricles. The actual pathology may be
the area of myocardium directly surrounding the AV node itself, or the problem may be in the
node. First degree block also frequently occurs in the presence of an acute inferior wall MI>
it may also occur as the result of increased vagal (Parasympathetic) tone or digitalis toxicity.

Whichever the problem, the delay in the conduction is apparent on ECG as an increased P-R
interval. The PR interval is shown in the figure below. The normal time for the P-R interval
is up to 0.20 seconds. If the interval is longer, first degree block is present (assuming no
other underlying arrhythmia is present as well).

Also, in the first degree block, every other aspect of the ECG must be normal. The QRS
interval is normal. The P-R interval is prolonged but constant. The P waves are identical and
precede each QRS complex. Each P wave is conducted to the ventricles. Again, the only
abnormality is that the P-R interval is prolonged. The heart rate is that of the underlying
atrial or sinus rhythm. The QRS complexes are usually normal with first degree block.
However, they may rarely be abnormal because of a preexisting bundle branch block.
Typically, the AV conduction ratio is 1:1, that is, a QRS complex follows each P wave.

First degree AV block usually produces no symptoms in the patient. However, this
condition can progress to a higher degree AV block. Because this condition may get worse,
patients are usually observed carefully. The person will have regular checkups and regular
EKG tracings and monitoring.

SECOND DEGREE AV BLOCK

This type of arrhythmia is divided into two categories:

The first is called Mobitz Type I or the Wenckebach Phenomenon.

The second is called Mobitz Type II AV Block

In general, both of these are more severe than the previously discussed first degree block. In
second degree block, the impairment is so great that some of the P waves fail to initiate a
ventricular contraction. In second degree block, the atrial impulses are usually of normal rate
and rhythm, and the QRS complexes are also normal. The term Mobitz is being used less and
the arrhythmias are simply being called Type I or Type II. However, Mobitz is still used by
many authorities.

MOBITZ TYPE I AV BLOCK

In this type of second degree block, there is a progressive increase in the P-R interval as
shown in the example. The P-R interval increases until the point that the P wave is totally
blocked and no QRS flows, and the beat is dropped. After the dropped beat, the cycle starts
over again. The P-R interval appears almost normal, and then continues to lengthen and the
cycle repeats itself. This type of second degree block is common in patients with an acute
inferior myocardial infarct, but it is generally considered the less serious type of second
degree block. It may disappear spontaneously. It may even be caused by excessive digitalis
dosing, and usually does not require a pacemaker. However, if the ventricular response is
very low, then atropine or isoproterenol may be used. This type of arrhythmia is not serious
by itself, but may increase to a more serious arrhythmia. The patient needs to be observed
and have regular checkups.

In this type of arrhythmia, the atrial rhythm is essentially regular. The ventricular rhythm is
irregular. The P waves are identical and precede the QRS complexes when they occur. The
P-R intervals gradually lengthen until a QRS complex fails to appear after a P wave (Non-
conducted P wave or Dropped Beat). Following the pause caused by the dropped beat, the
sequence begins again.
MOBTIZ TYPE II AV BLOCK

This type of second degree block is the more serious type. Essentially, there is a definite ratio
of blocked beats. Some P waves will not get through the AV node in order to initiate the
contraction of the ventricles. It can be every 5th beat which is dropped, very 4th beat, or
every 3rd beat, etc.

The more frequent the dropped beat, the more serious is the block. If the ratio is 4 to 1, the
patient may have not experienced any adverse symptoms. If the blocked beat is every other
beat (2:1 ratio) then the person probably will exhibit dizziness, fainting or other symptoms
and need immediate treatment. The more serious block, 2:1 ratio, requires immediate
treatment because this may lead to ventricular asystole and death.

THIRD DEGREE BLOCK (COMPLETE AV BLOCK)

Third degree block is complete or total blockage of all impulses through AV node. The atria
and ventricles beat totally independent of each other. The atrial rate and rhythm are usually
regular. If P waves are present, they may have originated in the SA node of from an ectopic
pacemaker in the atria. P wavers, atrial flutter, or atrial fibrillation waves may be present.
When present, they have no relation to the QRS complexes, appearing independently at a
rate different from that of the QRS complexes (atrioventricular (AV) dissociation). See
example below.

The pacemaker for the ventricles may be anywhere in the conduction system of the
ventricles. It may be in the AV node, Bundle of HIS, or bundle of Purkinje system. The
lower in the conduction system that the pacemaker is located, the slower the ventricular rate
will usually be. This slow rate is referred to s idioventricular rhythm. If the pacemaker for
the ventricle is high in the system, or even the AV node itself, the ventricular rhythm may be
sufficient enough that the patient will have no adverse effects. However, since the rate is
usually below 60 BPM, the patient usually exhibits Stokes-Admas attacks (syncopal attacks),
CHF or angina attacks.

QRS complexes are usually normal, but the QRS interval may be widened and/or lengthened
in some cases. The QRS complexes typically exceed 0.12 second and are bizarre if the
escape pacemaker site is in the ventricles or if the escape pacemaker site is in the AV
junction and a preexisting bundle branch block is present. However, the QRS complexes
may be normal (0.10 second or less), if the pacemaker site is above the bundle branches in
the AV junction and no bundle branch bock is present. Third degree AV block may be
transient and reversible. Some treatable conditions may cause this block and it may be
reversed. However, when the QRS complexes are wide and bizarre and the heart rate is in the
30 – 40 range, it is an indication that the condition is not reversible. These permanent block
conditions are usually cause by the anterior wall MI or chronic degenerative changes in the
bundle branches in the elderly. The treatment of third degree block is the immediate insertion
of a cardiac pacemaker, no matter what the cause of the block.

Fig: 3: Abnormal ECG patterns

7. BUNDLE BRANCH BLOCK

DEFINITION:

A delayed ventricular stimulation, usually due to blockage of impulses traveling through the
bundle of HIS.

ETIOLOGY:

This is a conduction defect in either the right or left branches of the bundle of HIS. Usually,
the cause is tissue damage.

CLINICAL IMPLICATIONS:

The arrhythmia itself is not dangerous. However, the cause of the damage is usually the
reason for concern. Usually there are no symptoms with bundle branch block (BBB). The
problem, as with other asymptomatic conditions, is usually detected upon routine physical
exams, or while the MD is examining the patient for a different complaint.

Right BBB may exist with no symptoms at all and virtually no evidence of disease present.
Left BBB is almost always associated with extensive tissue damage (infarcts) of the septal
area. Branches of the Bundle of HIS

1. Right Bundle Branch

2. Left Bundle Branch (2 Divisions)

a. Anterior-superior division

b. Posterior-inferior division

VENTRICULAR ARRHYTHMIAS

1. Premature Ventricular Contractions (PVC’s)

PVC’s are extra beats which occur from an ectopic focus on the ventricle wall. This focus is
usually below the bifurcation of the bundle of HIS. In the normal person these may be
caused by smoking, alcohol, or coffee ingestion. They usually are rare and inconsequential in
normal persons. PVC’s may also, and more frequently, occur as the result of an MI or due to
arteriosclerotic heart disease. This irritable spot on the myocardium sends out a powerful
electrical impulse which spreads across the ventricles, causing them to contract out of proper
sequence. In other words, the ventricles contract before they have had a chance to
completely fill with blood from the contraction of the atria.

PVC’s may be unifocal (from one spot on the ventricle wall) or they may be multifocal (from
two or more different spots [foci] on the ventricle wall). Obviously, the multifocal PVC is the
more dangerous condition; it indicates the general irritability of the myocardium and the
possibility of even more dangerous heart arrhythmias. Shown in the below illustration are
different types of PVC’s.

PVC’s may be single and isolated (rare), which are usually normal. They may also be more
frequent, occurring at regular intervals.

When they occur at regular intervals, they are called:

Bigeminy – every other beat.

Trigeminy – every third beat.

Quadrageminy – every fourth beat

If the beats occur less frequently than every fourth beat there is usually no regular pattern.
They will tend to be irregular in the pattern. However, it can be noted that PVC’s might
occur regularly, every fifth beat, sixth beat, etc.

If they occur more frequently than every 4th beat the condition can be serious and possibly
require treatment. Multifocal PVC’s are also more dangerous then unifocal. If they appear in
groups of two or more together (coupled), the situation could also be dangerous. In addition,
the most dangerous situation is called the R-on-T Phenomenon. When the PVC falls on a T
wave from the previous contraction, ventricular fibrillation and death can occur. During the
T wave (repolarization), heart muscle is very sensitive to outside stimulus thus a strong PVC
can send the myocardium into fibrillation. Treatment of PVC’s is complex. In the “normal”
situation, Lidocaine is administered to decrease the irritability of the myocardium. An
initially high intravenous dose (bolus) is given and then the patient is monitored on a lower
maintenance dose (intravenous drip). If the PVC’s continue after the Lidocaine is terminated,
the patient is maintained on an oral dose of some similar type drug.

A case where Lidocaine may not be used would be in Bradycardia. If the SA node rate falls
below 60 per minute, the heart may try to compensate by the use of PVC’s. Another case is
after carefully studying the ECG tracing and determining that the underlying arrhythmia is
Sinus Bradycardia, Lidocaine may not be used. The MD will usually give Atropine to
increase the SA node firing. This increase in the pulse rate will then give rise to the
termination of the inefficient PVC’s needed to maintain circulation.

2. VENTRICULAR TACHYCARDIA (V-TACH)

This is a very serious arrhythmia. Whenever three or more consecutive PVS’s are seen, at a
rate of 100 bpm or more, the term used is Ventricular Tachycardia (V. Tach). In the strictest
definition, V. Tach is the same as PVC’s, except that there are many of them in a row. The
onset and termination of V. Tach may be may be abrupt or not. V. Tach may occur in
paroxysms of three or more PVC’s separated by the underlying rhythm (non-sustained V
Tach or Paroxysmal Ventricular Tachycardia), or persist for a long period of time (sustained
ventricular tachycardia). The rhythm is usually regular, but it may be slightly irregular.

Bundle Branch Block, as stated, is abnormal conduction through the ventricles. If a block
exists in one of the bundle branches of the Bundle of HIS, the impulse will travel down the
branch to the opposite bundle first. Having activated this bundle, the impulse will then spread
through the septum to the ventricle on the other side of the block and then cause it to be
activated. The block may only affect one division on the left bundle branch.

3. VENTRICULAR FIBRILLATION

Ventricular Fibrillation (V. Fib) means sudden death. The blood pressure drops immediately
to zero and so does the cardiac output. The heart is merely quivering due to the rapid
multiple electrical discharges in the myocardium. V. Fib is one of the most common causes
of cardiac arrest. It usually occurs in the presence of significant cardiac disease. It occurs
most commonly in coronary artery disease, myocardial ischemia, acute myocardial infarction,
and third degree AV Block with a slow ventricular response. V. Fib may also occur in
cardiomyopathy, mitral valve prolapsed, cardiac trauma (blunt trauma), and in digitalis
toxicity. V. Fib may also occur during anesthesia, cardiac and noncardiac surgery, cardiac
catheterization, during cardiac pacing, following cardio version, accidental, or non-accidental
electrocution.

ARRHYTHMIA DETERMINATION
This is one of the most important sections of this course. Interpretation of the ECG must be
done in a logical sequence in order to best serve the patient. There are many different
approaches to the interpretation of the ECG, but in this section we will present a “common
sense” approach. If you are responsible for a patient who is being monitored, you want to be
able to recognize any arrhythmia that may be life-threatening. You want to be able to do that
as fast as possible; it may save the life of your patient. As you read and study these steps,
remember that they may not apply to every patient in every situation. However, you should
always be deliberate and methodical when you interpret the ECG.

PHASE I: ASSESSMENT

a. Assess patient symptoms, if and, and vital signs.

b. Assess leads to the patient (leads must be in proper placement).

c. Assess obvious abnormalities of ECG (rate, rhythm).

In the assessment phase, the nurse must quickly note any symptoms. The symptoms will
determine if the arrhythmia is severe or not. The vital signs are important. At the same time
you are assessing the patient, look at the ECG to determine if there are any gross arrhythmias.
If so, you can then take the appropriate action. The patient may need immediate resuscitation
or they may be able to wait for treatment.

PHASE II: ECG COMPONENTS (Examine the Individual Components of the EKG)

a. Step One: Identity the QRS complex.

b. Step Two: Determine the heart rate.

c. Step Three: Determine the ventricular rhythm.

d. Step Four: Identify the P. Waves.

e. Step Five: Determine the P-R or R-P interval.

f. Step Six: Determine the pacemaker rate.

PHASE III: DETERMINE THE ARRHYTHMIA

a. Atrial arrhythmia.
b. Ventricular arrhythmia.

Once you have identified the abnormal component of the ECG, you then name the
arrhythmia. If the abnormality is in the atria (P wave), then identify the arrhythmia. If the
abnormality is in the ventricle, then identify the arrhythmia.

PHASE IV: ACTION

a. Immediate action.

b. Long-term action/intervention

As stated above, if the arrhythmia is immediately life-threatening, then immediate action

must be taken. However, in most nursing situations the action will involve notifying the MD
and then treating the arrhythmia with the appropriate drug. As you proceed through each of
the steps, you must continually be aware of the changes in the patient’s condition and of
possible intervention. Each hospital has a different protocol for dealing with arrhythmias.
Always consider your hospital’s policy and procedure and use your common sense when
dealing with these potentially fatal arrhythmias.

CONCLUSION:

The normal values referred to in this discussion have been drawn from our experience at
Children’s Hospital Boston and the classic publications of Davignon and colleagues,8
Garson,9 and Fisch.10 Data are abstracted for quick reference in Table 12-1. The ECG
should be read in a systemic fashion, beginning with measurements of axes and intervals,
followed by waveform analysis, all of which must be synthesized into a final impression
based on history and physical examination. ECG inturn helps in detection of abnormal wave
patterns and provide immediate and emergency treatment.

BIBLIOGRAPHY:

1. Lewis T. The Mechanisms and Graphic Registration of the Heart Beat [preface]. London:
Shaw and Sons, 1925:vi.

2. Nadas AS. Electrocardiography. In Pediatric Cardiology. Philadelphia: WB Saunders,

1957:42.
3. Garson A. Recording the sequence of cardiac activity. In The Electrocardiogram in Infants
and Children. Philadelphia: Lea & Febiger, 1983:19–48.

4. Gilmore RF, Zipes DP. Cellular basis for cardiac arrhythmias. Cardiol Clin 1:3, 1983.

5. Plonsey R. The biophysical basis for electrocardiography. In Liebman J, Plonsey R,

Gillette RC (eds). Pediatric Electrocardiography. Baltimore: Williams & Wilkins, 1982:1–14.

6. Zipes DP. Genesis of cardiac arrhythmias: Electrophysiological considerations. In

Braunwald E (ed). Heart Disease. Philadelphia: WB Saunders, 1984:605–620.